The proposed project can reasonably be expected to provide a detailed understanding of the mechanisms of pathogenesis of the associated diseases of lens-induced endophthalmitis and sympathetic ophthalmia as well as provide information on the basis of their relationship. The revised proposal is based upon the development of useful experimental models of both sympathetic ophthalmia and lens-induced endophthalmitis which may now be employed to evaluate the specific immunopathogenic mechanisms involved in these diseases, to investigate treatment programs as well as to test some fundamental theories of autoimmunity involving both immune complex of presumably cell mediated effector responses. The effector mechanism in lens-induced endophthalmitis appears to be immune complex disease but the roles of cellular hypersensitivity as well as the pathogenesis of the granulomatous response require additional evaluation. The effector mechanism in sympathetic ophthalmia appears to involve cell mediated hypersensitivity but the relative roles of T and B cells remain to be established more rigorously. We propose to investigate the pathogenesis and interrelationship of these diseases in a coordinated series of clinical experimental studies designed to isolate the contribution of specific immunopathogenic mechanisms. Immunologic indices will be related to clinical as well as light and electron microscopic observations with particular attention focused on both clinical applicability as well as testing for basic theories of autoimmunity.